Histopathology 15 - Cerebrovascular disease and Trauma Flashcards

1
Q

What are the 2 main types of cerebral oedema?

A

Vasogenic (due to disrupted BBB)
Cytotoxic (due to hypoxia/ ischaemia)

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2
Q

What is the difference between communicating and non-communicating hydrocephalus?

A
Communicating = problem with CSF resorption into venous sinuses 
Non-communicating = Due to obstruction in flow
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3
Q

What is the normal range for ICP in a supine adult?

A

7-15mmHg

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4
Q

What is the most important contraindication to lumbar puncture?

A

Pailloedema

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5
Q

What is the most common site for non-traumatic intra-parenchymal haemorrhages?

A

Basal ganglia

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6
Q

What is the biggest risk factor for non-traumatic intra-parenchymal haemorrhage?

A

Hypertension

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7
Q

When do congenital arteriovenous malformations tend to become symptomatic?

A

Between 2nd and 5th decade

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8
Q

What is the management of ruptured congenital arteriovenous malformation?

A

Surgically remove if poss, this may be radiosurgery
Embolise (to stop bleeding)

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9
Q

What is a cavernous angioma?

A

Hemangioma (vascular tumour), which causes a slowing of blood flow through “caverns”

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10
Q

When do cavernous angiomas become symptomatic?

A

When they bleed - which is at low pressure and usually >50 years

so essentially after congenital AVMs

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11
Q

What is the most common site of haemorrhage in subarachnoid haemorrhage?

A

Berry aneurysm rupture
80% at internal carotid artery bifurcation

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12
Q

What is the key symptom of subarachnoid haemorrhage?

A

Sudden onset severe ‘thunderclap’ headache

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13
Q

At what size of Berry aneurysm is the risk of rupture greatest?

A

>6mm

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14
Q

How can Berry aneurysms be fixed?

A

Platinum coiling

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15
Q

In which cerebral artery are infarctions most likely?

A

Middle cerebral artery

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16
Q

What % of TBI patients make a good recovery?

A

31%

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17
Q

What are the clinical signs of skull fracture?

A

Otorrhoea and rhinorrhoea with straw-coloured fluid

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18
Q

What is contusion?

A

Brain collision with skull which causes surface bruising

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19
Q

Which structures are mosta affected by traumatic diffuse axonal injury?

A

Midline structures eg corpus callosum

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20
Q

Two types of cerebral infarction

A

Stroke and TIA

TIA is an important predictor of stroke

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21
Q

Commonest vascular territory affected by stroke

A

Middle cerebral artery

22
Q

Vascular territories affected by TIA

A

Can be any

characteristically embolic atherogenic debris from the carotid artery travels to the ophthalmic branch of internal carotid

23
Q

Management of stroke

A

Aspirin +/- dipyridamole

Thrombolytics (if <3h from event)

+/- carotid endarterectomy

Long term: treat HTN, ↓lipids, anticoag

Main imaging: CT-head non-contrast

24
Q

Treatment of TIA

A

Aspirin + dipyridamole
+/- carotid endarterectomy

Long term: treat HTN, ↓lipids, anticoagulants

**same as stroke except for thrombolytics

25
ACA stroke
contralateral leg paresis, sensory loss, cognitive deficits (e.g. apathy, confusion, and poor judgment) \*\*essentially leg\>arm
26
MCA stroke signs
contralateral weakness and sensory loss of face and arm • cortical sensory loss • may have contralateral homonymous hemianopia or quadrantanopia • if dominant (usually left) hemisphere: aphasia • if non-dominant (usually right) hemisphere: neglect • eye deviation towards the side of the lesion and away from the weak side \*\*doesn't affect legs like ACA
27
PCA stroke signs
contralateral hemianopia or quadrantanopia • midbrain findings: CN III and IV palsy/pupillary changes, hemiparesis • thalamic findings: sensory loss, amnesia, decreased level of consciousness • if bilateral: cortical blindness or prosopagnosia • hemiballismus
28
Basilar artery stroke signs
1. Proximal (usually thrombosis): impaired EOM, vertical nystagmus, reactive miosis, hemi- or quadriplegia, dysarthria, locked-in syndrome, coma 2. Distal (usually embolic, i.e. top of the basilar sydrome): somnolence, memory and behavior abnormalities, oculomotor deficit
29
PICA signs
PICA (lateral medullary or Wallenberg syndrome): ipsilateral ataxia, ipsilateral Horner’s, ipsilateral facial sensory loss, contralateral limb impairment of pain and temperature sensation, nystagmus, vertigo, nausea/vomiting, dysphagia, dysarthria, hiccups
30
Lacunar infarct: where is this?
(deep hemispheric white matter; involving deep penetrating arteries of MCA, circle of Willis, basilar, and vertebral arteries) 1. Pure motor hemiparesis (posterior limb of internal capsule): contralateral arm, leg, and face 2. Pure sensory loss (ventral thalamic): hemisensory loss 3. Ataxic hemiparesis (ventral pons or internal capsule): ipsilateral ataxia and leg paresis 4. Dysarthria-clumsy hand syndrome (ventral pons or genu of internal capsule): dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness
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32
Types of non-traumatic haemorrhage
Intraparnehchymal Subarachnoid
33
Most common cause of intraparenchymal haemorrhage
50% due to HTN
34
Common site of intraparenchymal haemorrhage
Basal ganglia
35
Most common cause of subarachnoid haemorrhage
85% of ruptured berry aneurysms
36
Most common location of SAH
Internal carotid artery bifurcation
37
What causes charcot-bouchard microaneurysms
Non-tramautic intraparnechymal haemorrhage
38
RF of SAH
F\>M, usually \<50yrs, → thunderclap headache, vomiting and LoC, ↑in PKD, Ehler’s Danlos and Pts with Aortic Coarctation. Also associated with vascular abnormalities incl AV malformations, capillary telangiectasias, venous and cavernous angiomas, Ehlers Danlos.
39
Types of traumatic haemorrhage
Extradural Subdural Traumatic parenchymal injury
40
Extradural haemorrhage
Skull fracture, ruptured middle meningeal artery → rapid arterial bleed, lucid interval then LoC,
41
Which type of haemorrhage give syou lucid interval?
Extradural haemorrhage
42
Subdural haemorrhage
Prev history of minor trauma → damaged bridging veins with slow venous bleed, often elderly/alcoholic, associated with brain atrophy, fluctuating consciousness
43
Types of traumatic parenchymal injury
Concussion: Transient LoC and paralysis, recovery in hours or days ● Diffuse axonal injury: Vegetative state, post traumatic dementia ● Contusions: When brain contacts skull +/- fracture. ● Traumatic intracerebral haemorrhage
44
Coup vs contracoup
Coup - where the impact occurs Contracoup - opposite to region impact
45
Causes of increased ICP
: Caused by oedema, space occupying lesion (e.g. tumour, abscess) or both → brain herniation.
46
Six types of brain herniation
Uncal, Central (transtentorial), Cingulate (subfalcine), Transcalvarial, Upward, Tonsillar.
47
Causes ofbacterial meningitis by age
**Neonatal to 3 months**: Group B streptococcus (GBS) early (90% day 1–5) or late (10% 6 days–3 months), E. coli, Listeria monocytogenes. **• 1 month to 6 years:** Neisseria meningitidis (meningococcus), Streptococcus pneumoniae,Haemophilus influenzae type B (Hib). **• \>6 years**: N. meningitidis (14–25 years), Strep. pneumoniae, mumps (pre-MMR). **• Mycobacterium tuberculosis:** Can cause TB meningitis at all ages. Most common in children 6 months–6 years. **• Older adults**: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b (Hib), group B Streptococcus, Listeria monocytogenes
48
Viral causes of meningitis
Enteroviruses (80%), cytomegalovirus (CMV), arbovirus. Herpes simplex virus (HSV) is more likely to cause encephalitis 2. Herpes simplex most common in adults. All others most common in children and infants.
49
meningitis LP finidngs
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51
Which lobe of the brain is affected by HSV encephalitis?
Temporal lobe